Hall J E, Guyton A C, Brands M W
Department of Physiology & Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Kidney Int Suppl. 1996 Jun;55:S35-41.
In all forms of hypertension, including human essential hypertension, pressure natriuresis is abnormal because sodium excretion is the same as in normotension despite increased arterial pressure. Considerable evidence indicates that this resetting of pressure natriuresis plays a key role in causing hypertension, rather than merely occurring as an adaptation to increased blood pressure. Because human essential hypertension is a heterogeneous disease, it is likely that multiple neurohumoral and intrarenal defects contribute to abnormal pressure natriuresis and increased blood pressure. Physiological studies have shown that renal abnormalities that cause increased distal and collecting tubule reabsorption, decreased glomerular filtration coefficient or loss of nephrons also cause decreased slope of pressure natriuresis (salt-sensitive hypertension), whereas increased preglomerular resistance causes a parallel shift of pressure natriuresis (salt-insensitive hypertension). Comparison of the characteristics of pressure natriuresis (such as salt-sensitivity of blood pressure) in hypertensive subjects with those forms of experimental hypertension of known origin can provide insight into the etiology of human hypertension. With long-standing hypertension, pathological changes in the glomeruli and renal arterioles may further shift pressure natriuresis and exacerbate hypertension.
在所有形式的高血压中，包括人类原发性高血压，压力性利钠作用是异常的，因为尽管动脉血压升高，但钠排泄与正常血压时相同。大量证据表明，这种压力性利钠作用的重置在导致高血压中起关键作用，而不仅仅是作为对血压升高的一种适应性反应而发生。由于人类原发性高血压是一种异质性疾病，多种神经体液和肾内缺陷可能导致压力性利钠作用异常和血压升高。生理学研究表明，导致远曲小管和集合管重吸收增加、肾小球滤过系数降低或肾单位丢失的肾脏异常也会导致压力性利钠斜率降低（盐敏感性高血压），而肾小球前阻力增加会导致压力性利钠作用平行移位（盐不敏感性高血压）。将高血压患者的压力性利钠特征（如血压的盐敏感性）与已知病因的实验性高血压形式进行比较，可以深入了解人类高血压的病因。长期高血压会导致肾小球和肾小动脉的病理变化，可能进一步使压力性利钠作用移位并加重高血压。
